Anti-Peat High-Salt Augments Aldosterone Toxicity Despite Lowered Plasma-Readings

Discussion in 'Debate - Anti-Peat' started by Tristan Loscha, Oct 19, 2019.

  1. Tristan Loscha

    Tristan Loscha Member

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    High-Salt Augments Aldosterone Toxicity Despite Lowered Plasma-Readings.

    Blood-LVL-Aldosterone gets lowered by sodium,but apparently sensitivity rises,augmenting
    damage.Sodium is truly almost a micronutrient,with intakes as low as 500mg-1500mg,in indigenous tribes,lower than
    magnesium,lower than calcium,severely lower than potassium.

    Thoughts?



    Effect of aldosterone and mineralocorticoid receptor blockade on vascular inflammation
    Hylton V Joffe, Gail K Adler
    Heart failure reviews 10 (1), 31-37, 2005
    Aldosterone, the final product of the renin-angiotensin-aldosterone system, is classically viewed as a regulator of renal sodium and potassium handling, blood volume, and blood pressure. Recent studies suggest that aldosterone can cause microvascular damage, vascular inflammation, oxidative stress and endothelial dysfunction. In animal models, aldosterone-mediated vascular injury in the brain, heart, and kidneys leads to stroke, myocardial injury, and proteinuria. These effects may be modified by dietary salt intake; aldosterone-mediated vascular damage is increased in susceptible animals fed a high-salt diet compared to a low-salt diet despite lower plasma aldosterone levels on the high-salt diet. In humans, there is a growing literature supporting the adverse effects of aldosterone in heart failure, hypertension, left ventricular hypertrophy, and renal disease. Aldosterone receptor antagonists are beneficial even in patients on angiotensin converting enzyme inhibitors and attenuate aldosterone-mediated vascular injury by mechanisms that appear to be independent of changes in systolic blood pressure. This review focuses on the adverse effects of aldosterone on the vascular system and describes our current understanding of the underlying mechanisms for this injury.

    Furthermore,
    Sodium-related:



    Dietary salt intake is related to inflammation and albuminuria in primary hypertensive patients
    R Yilmaz, H Akoglu, B Altun, T Yildirim, M Arici, Y Erdem
    European Journal of Clinical Nutrition 66 (11), 1214, 2012
    RESULTS:
    Systolic and diastolic BP measurements of patients were similar in the three salt-intake groups. CRP and urinary albumin levels were significantly higher in high-salt-intake group compared with medium-and low-salt-intake groups (P= 0.0003 and P= 0.001, respectively). CRP was positively correlated with 24-h urinary sodium excretion (r= 0.28, P= 0.0008) and albuminuria, whereas albuminuria was positively correlated with 24-h urinary sodium excretion (r= 0.21, P= 0.0002). Multiple regression analysis revealed that urinary sodium excretion was an independent predictor of both CRP and albuminuria.
    CONCLUSIONS:
    These findings suggest that high salt intake is associated with enhanced inflammation and target organ damage reflected by increased albuminuria in treated hypertensive patients independent of any BP effect.
     
  2. lampofred

    lampofred Member

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    I think RP said many of the negative effects attributed to sodium excess are actually due to calcium deficiency. Calcium and sodium have antagonistic effects, so if you increase sodium then calcium also has to go up to match (otherwise you get calcium deficiency symptoms). Then you get the aldosterone-lowering effect of salt without the inflammatory effects.

    That's my guess as to how to explain the study results.
     
  3. OP
    Tristan Loscha

    Tristan Loscha Member

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    Interesting.
    Another Thing about intake of Sodium is that it seems that in hypothyroidism there is hyponatremia,
    meaning Low-Blood-Level,but increased Residual-Sodium in theTissues,excretion doesnt work,because
    of renal disorder.
    But what happens to the excess Sodium in the tissue?I read a lot about sodiums Role in augmenting
    autoimmune-disease activity in Enimal and in Human by induction of a special T-Helper-Cell-Lineage called TH17.It does so very potently,destroying Self-Tolerance.For Depression there were also reports of
    heightened Bodystorage of Sodium,and Major Depression and Hypertension are both inflammatory diseases.

    I have the severe Hunch that Sodium,which modern-day intake is possibly ridiculous High,is Driving Inflammation
    for lots of Folk,all around the World.If someone Supplements anything,its always NaCl.Wisdom or Deranged Metal-Taste-Mania?
     
  4. Kunstruct

    Kunstruct Member

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    Always liked salt.
    So far, never been more than 1.X TSH far from any hypothyroidism, typical blood pressure is 110-115, far from any hypertension.
    Avoiding salt seems to not benefit me so far.
     
  5. OP
    Tristan Loscha

    Tristan Loscha Member

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    Are Sensations of Health attached to that liking or is it the Taste though?
    Salt isnt increasing Blood Pressure.the effect of Sodium is induction
    of vascular autoimmunity in Hypertensives,also Salt-Sensitive Hypertension.
     
  6. OP
    Tristan Loscha

    Tristan Loscha Member

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    All Yuge Mystery-Deseases have inflammation in common,of autoimmunity appearance.
    Hypa-Tension,Multiple Sclerosis,Acne,Psoriasis,Irrtable Bowel Syndrome,Colitis,Alzheimer,
    Parkinsons,etcetc.all have Th17 Pathology in common,and already "Normal" to High Salt intakes are
    increasing the Maturation of these Bad Boys so badly.I believe that Sodium is a micronutrient with low
    "therapeutic breadth" between 500mg-to-1500mg per day.
     
  7. OP
    Tristan Loscha

    Tristan Loscha Member

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    :
    Th17 Cells Induce Dopaminergic Neuronal Death via LFA-1/ICAM-1 Interaction in a Mouse Model of Parkinson’s Disease
    Abstract

    T helper (Th)17 cells, a subset of CD4+ T lymphocytes, have strong pro-inflammatory property and appear to be essential in the pathogenesis of many inflammatory diseases. However, the involvement of Th17 cells in Parkinson’s disease (PD) that is characterized by a progressive degeneration of dopaminergic (DAergic) neurons in the nigrostriatal system is unclear. Here, we aimed to demonstrate that Th17 cells infiltrate into the brain parenchyma and induce neuroinflammation and DAergic neuronal death in 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)- or 1-methyl-4-phenylpyridinium (MPP+)-induced PD models. Blood–brain barrier (BBB) disruption in the substantia nigra (SN) was assessed by the signal of FITC-labeled albumin that was injected into blood circulation via the ascending aorta. Live cell imaging system was used to observe a direct contact of Th17 cells with neurons by staining these cells using the two adhesion molecules, leukocyte function-associated antigen (LFA)-1 and intercellular adhesion molecule (ICAM)-1, respectively. Th17 cells invaded into the SN where BBB was disrupted in MPTP-induced PD mice. Th17 cells exacerbated DAergic neuronal loss and pro-inflammatory/neurotrophic factor disorders in MPP+-treated ventral mesencephalic (VM) cell cultures. A direct contact of LFA-1-stained Th17 cells with ICAM-1-stained VM neurons was dynamically captured. Either blocking LFA-1 in Th17 cells or blocking ICAM-1 in VM neurons with neutralizing antibodies abolished Th17-induced DAergic neuronal death. These results establish that Th17 cells infiltrate into the brain parenchyma of PD mice through lesioned BBB and exert neurotoxic property by promoting glial activation and importantly by a direct damage to neurons depending on LFA-1/ICAM-1 interaction.
     
  8. OP
    Tristan Loscha

    Tristan Loscha Member

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    "HIGHLIGHTS"

    Highlights

    Increased numbers of T cells are detected in PD postmortem midbrains


    Increased frequencies of IL-17-producing T cells are found in PD patients’ blood


    T cells induce neuronal death in PD revealed by human autologous iPSC-based model


    Neuronal cell death is mediated by IL-17–IL-17R signaling and activation of NFκB

    Th17 Lymphocytes Induce Neuronal Cell Death in a Human iPSC-Based Model of Parkinson’s Disease



    Summary
    Parkinson’s disease (PD) is a neurodegenerative disorder characterized by the progressive degeneration of midbrain neurons (MBNs). Recent evidence suggests contribution of the adaptive immune system in PD. Here, we show a role for human T lymphocytes as cell death inducers of induced pluripotent stem cell (iPSC)-derived MBNs in sporadic PD. Higher Th17 frequencies were found in the blood of PD patients and increased numbers of T lymphocytes were detected in postmortem PD brain tissues. We modeled this finding using autologous co-cultures of activated T lymphocytes and iPSC-derived MBNs of sporadic PD patients and controls. After co-culture with T lymphocytes or the addition of IL-17, PD iPSC-derived MBNs underwent increased neuronal death driven by upregulation of IL-17 receptor (IL-17R) and NFκB activation. Blockage of IL-17 or IL-17R, or the addition of the FDA-approved anti-IL-17 antibody, secukinumab, rescued the neuronal death. Our findings indicate a critical role for IL-17-producing T lymphocytes in sporadic PD.

    ------------------------------------------------------------------------------------------------------------------------------------------------------------------------

    HI SODIUM shifts the specialization of naive T-Helper-Cells (Th1,Th2,Th17) to the highly inflammatory TH17
    phenotype,which produces high amounts of toxic cytokines,the whole hog,and acts potently anti-anti-inflammatory.
    TH17 helper t-cells secrete IL17 which is on topic in the study.this pathway is reserved for severe intracellular infection,
    but the salt dispensing saltingmaniac decides for us instead.
     
  9. OP
    Tristan Loscha

    Tristan Loscha Member

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    Another Salt Study,Acne:


    Salty and spicy food; are they involved in the pathogenesis of acne vulgaris? A case controlled study
    MA El Darouti, OA Zeid, DM Abdel Halim, RA Hegazy, D Kadry, DI Shehab, HS Abdelhaliem, MA Saleh
    Journal of cosmetic dermatology 15 (2), 145-149, 2016
    Background
    Many studies have suggested a strong relation between diet and acne. Many patients with acne believe that spicy and salty foods exacerbate acne.
    Aim
    To assess the relationship between the dietary intake of salty and spicy food and the onset, severity, duration of acne.
    Methods
    Two hundred patients with acne vulgaris and 200 age‐ and gender‐matched controls were subjected to a detailed questionnaire taking, clinical examination and dietary assessment through using “24 h recall” method. Sodium content of the 24‐h food intake was computed by a computer program connecting participants' dietary information to the food composition table of National Nutrition Institute data base.
    Results
    Patients with acne consumed significantly higher daily amounts of sodium chloride (NaCl) (median 3367.54 mg) compared to the controls (median 2271.8 mg) (P < 0.001). A negative correlation between the amount of NaCl in the diet of patients with acne and the age of onset of acne lesions was detected (r = −0.216, P = 0.031). However, neither salty nor spicy food correlated with duration or severity of the disease.
    Conclusion
    Consumption of salty foods was significantly higher among patients with acne compared to acne free subjects, making the consumption of salty food a possible participating factor in the development of acne.
     
  10. OP
    Tristan Loscha

    Tristan Loscha Member

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    Also:satellite:

    https://www.researchgate.net/profile/Andrei_Pernambuco/publication/256489355_Increased

    _levels_of_IL-17A_in_patients_with_fibromyalgia/links/0a85e5321ecdd6c5fd000000.pdf

    Fibromyalgia and cytokines
    I Rodriguez-Pintó, N Agmon-Levin, A Howard… - Immunology letters, 2014 - Elsevier
    IL-17 is the major cytokine released by Th17 cells and it has a major role in the

    pathogenesis
    of inflammatory and autoimmune diseases … [27] found increased levels of IL-17A in

    patients with
    fibromyalgia and correlated their levels with increased levels of IL-2, IL-4, IL-10,

    TNF-a.



    The analyses showed that fibromyalgia patients present increased
    levels of IL-17A. They also revealed
    that plasma concentrations of IL17A
    positively correlate with levels of IL-2,
    IL-4 and IL-10, TNF and IFNγ.





    Increased salt intake above a approximated physiologic threshold of 500mg-1500mg Na

    per day
    is responsible for polarization of initally "naive" T-helper cells (Th) to the highly

    aggressive Th17 Phenotype,
    which is orthodoxically induced by severe intracellular infection like

    tuberculosis.Excess Na can do all of that without infection though.
    "Osmotically neutral sodium retention".
     
  11. tankasnowgod

    tankasnowgod Member

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    This whole idea makes no sense. The whole reason that aldosterone rises in the first place is to conserve sodium when intake is inadequate.
     
  12. tankasnowgod

    tankasnowgod Member

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    High compared to what? Sodium intakes have dropped dramatically since the early 20th century, and were far, far higher in the 16th-18th century, when salt was primarily used as preservative. I think salt intakes were almost 10 times higher then.
     
  13. tankasnowgod

    tankasnowgod Member

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    Those diseases have been on the rise while salt intake has maintained or fallen, population wise. I would suggest a bigger culprit is added iron, an element that has been dramatically on the rise over the years, that has a causal role in Alzheimers, Parkinsons, Hypertention, and could certainly contribute to IBS and Colitis, when it's ingested as the raw metal. Oh, and it's highly inflammatory as well. I think you are barking up the wrong tree with salt.
     

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  14. nwo2012

    nwo2012 Member

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    Exactly what I was going to reply. And even worse is the ridiculous amounts of water people drink to be 'healthy'.
    Its like the BS that saturated fat and sugar consumption have skyrocketed, no only PUFA consumption has soared. Im sure the diets fed in these studies are deficient of many nutrients and of course PUFA laden. You can make any essential nutrient look bad in the wrong context, which is why we eat correctly 99.9% of the time. The OP is on a mission but the whole idea is pure BS.
     
  15. OP
    Tristan Loscha

    Tristan Loscha Member

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    It doesnt have to be a wrestling match between these 2 micro-villains.
    Consider this:"im smart, using my ferrumdispenser,because it was used for conservation"(lack of fridge).
    Consider that:For natural selection,there has to be death or infertility to select for traits.
    Hi-Salt just doesnt kill quick enough,and doesnt make infertile fast enough.
    So in my view,there just was no selection for maxemum-sodium-tolerance.
    We tolerate(yield) because we (our kidneys,and inner,salted to teh gill cellcompartiments.)can.
    And because we have to,because salt tastes funny on my tongue.
    Ever see dark ages middle ages Paintings.Maybe they look so wretched because they are salted to them gills!
    It was never about Bloodpressure.Sodium induces autoimmune-recognition of the host-vasculature.
    Na-SGK1-IL23R-IL23-TH17-IL17.All mystery-diseases have this column in common.
     
  16. tankasnowgod

    tankasnowgod Member

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    It's not a wrestling match, so much as a complete and total lack of evidence that higher salt intakes are even somewhat dangerous, never mind deadly.

    And Sodium does NOT "induce autoimmune-recognition of the host-vasculature."
     
  17. OP
    Tristan Loscha

    Tristan Loscha Member

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    Bro,you drink water all day,peeing all day.its for sodium clearance,and maybe chlorine elimination induced
    low grade metabolic acidosis.(renal Bicarbonate wasting)
    The actual true salt that is worthy is Potassium,and sodium is a micro like Magnesium.
    We never changed.Also,Aldosterone in Humans is for Potassium clearance,but im too lazy to collect proof.
     
  18. Terma

    Terma Member

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    You have interesting resources about the TH17 autoimmunity, though I'm skeptical about reasons for intracellular salt accumulation since there are several. I have not read these studies. Have you seen them anywhere make a distinction between sodium and chloride?
     
  19. OP
    Tristan Loscha

    Tristan Loscha Member

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    Yes,i do saw them make the distinction.Salt compound (NaCl) is from different angles a problem.The autoimmunity one.
    A Hallmark study came around 2013,proof that Sodium-"pressure(tonicity)" had an sensing element,
    which is SGK1,serum glucocorticoid Kinase 1,and they were firm about all that.
    "They" have the entire cascade down and proofed the dependency of every following step of each step before in the chain.
    Epidemiological proofing is indeed highly troubled.I was in on the Hi-Salt Carousel myself,but now im not so sure anymore.
    The effect strength of going between Lo-Mid-Hi Sodium,for animal and Hueman alike,is pretty mindblowing tbh.
    Lipid Peroxidation,a measure of how fast your Fat is rotting,cut by 50 percent after 2 weeks going from high or even mid
    salt to Lo-Salt(physiologic salt,kidney diet).MS,Parkinson,Psoriasis,Rheumathoid arthritis,Gullaine barre syndrome,
    much,much more,all have Th17 pathology in common,and Sodium is powerfully able to polarize neutral T-helper cells
    in the Th17 conformation.Lineage:Th1,Th2,Th17.Th17 pumps out insane cytokines,initiates NFKB like no bodys business.
    One thing about Salt accumulation.Keywords would be Osmotically neutral Sodium retention,
    that is an important event it seems.Cortisol-stress is ramping up the retention-cascade bigly,or so it seems.
     
  20. nwo2012

    nwo2012 Member

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    Firstly i never directly drink water only whats found in OJ, milk, coffee or foods. Secondly I dont urinate that often actually and its never clear like the 'healthy' people. Thirdly, as before, in the context of the average diet, any nutrient can be proven to he 'harmfull' but its not really proof at all. In a nutrient dense diet, one doesnt need to use NaCl sparingly. Thats context and its the RP way.
    Im not recommending the average sheeple increase its intake or sugar or any other nutrient because basically they are FUBAR.
     
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